As a result, the ability of CD8+ T cells to induce apoptosis in tumor cells via the FAS‐FASL pathway was markedly diminished.[44] The activation of the oncogenic RAS/MEK/ERK signaling pathway, driven by various KRAS mutations, stabilized both the mRNA and protein of PD‐L1.[43, 45] KRAS G12V was reported to upregulate PD‐L1 expression via the TGF‐β/ epithelial‐mesenchymal transition (EMT) signaling pathway.[46] However, the regulation of PD‐L1 expression was complex, and its association with KRAS mutations was not always positive. This evidence concerns the gene CD8A and neoplasm.